Hair growth is not continuous but rather cyclic, with alternating periods of growth `anagen` and rest `telogen`. In the scalp, the anagen phase lasts about 6 years and the telogen phase about 4 months. The growth of scalp hair is not synchronous, and the rate of growth is about 0.4 mm per day. About 90 percent of the more than 100,000 scalp hairs are growing (anagen), so that 50 to 100 hairs are shed daily as they are pushed out at the onset of a new hair cycle. These telogen hairs are also called club hairs because their ends are surrounded by visible clumps of keratinized cells.
The human skin has two kinds of hair. The terminal hairs are long, thick, and pigmented, while the vellus hairs are short, thin, and poorly pigmented. The terminal hairs can be easily seen with the unaided eye (scalp, beard, etc.) while the vellus hairs are only readily visible with magnification.
Common baldness is seen in the vast majority of adult males and is considered physiologic and part of the aging process. Since the degree, intensity, and age of onset of hair loss shows marked individual variations the most severe cases require the reassurance and understanding of the physician. Although several patterns of common baldness have been described in males, the recession of the hair line in the frontal region is by far the most common early finding. Eventually, alopecia develops on the vertex and as the two borders of alopecia advance, a semilunar configuration of hair loss develops. Besides the loss of hair, the length and diameter of each hair will be reduced in the adjacent areas even though the follicles remain intact.
In women, on the other hand, androgenetic alopecia is characterized by diffuse thinning over the vertex, parietal and temporal regions, but there is normal retention of the frontal hair line and the occipital zone is spared.
The cause of baldness is not well-established but a multifactorial form of inheritance has been suggested, which means that the loss is the result of the interaction of several genes with environmental factors. Genetically predisposed hair follicles seem to become the target for androgenic hormones and these follicles are programmed to become progressively smaller in size and to have shorter periods of growth. In the end stage only fine vellus hairs remain. It is not known how the androgens work or even whether the target tissue is the hair bulb or the supporting dermal components. There is no difference, for example, in the excretion of 17-ketosteroids or the blood levels of testosterone between normal balding and nonbalding individuals. The clinical difference between male and female pattern baldness is probably a function of the female genes, since it is believed that the same pathogenic mechanism applies to both.
Androgenetic alopecia can be distinguished from several other varieties of alopecia by etiologic diagnosis.
Telogen effluvium is a transient, reversible, diffuse shedding of hair in which a high percentage of hair follicles enter the telogen phase prematurely as a result of physical or mental illness. Among the most important factors incriminated are childbirth, high fever, hemorrhage, sudden starvation, accidental or surgical trauma, severe emotional stress, and certain drugs.
The diffuse shedding of telogen effluvium is not apparent for 2 to 3 months after the traumatic event and for that reason it is important to investigate in the history the above factors since the patient is usually unaware of the relationship. Although the hair loss is usually not excessive or prolonged enough to produce thinning of hair, in specific instances when the insult is prolonged thinning may become clinically apparent.
Alopecia areata is an immunologic alopecia characterized by the abrupt onset of sharply defined areas of hair loss. In mild cases, the process can be discovered accidentally by hairdressers or other persons examining the scalp of a patient, since hair loss can be clinically evident. In more severe cases, the patient may complain of excessive shedding of hair with large areas of the scalp completely devoid of hair. In the most severe cases, the scalp will develop total hair loss (alopecia totalis) or the hair loss will involve the whole body surface (alopecia universalis).
Although the disease affects any age, the higher incidence occurs in younger persons in whom 33 percent of the cases start by age 20. Only 25 percent of affected patients are over 40 years of age. There is no sex preference. Familial occurrence is between 10 and 20 percent and a familial tendency seems to be associated with a worse prognosis.
Most of the patients will run an unpredictable and relapsing course with multiple episodes of hair loss and regrowth. Only about 20 to 30 percent will have a single reversible episode. Regrowth of hair is common within several months, but in many instances is not complete and relapses are common.
Alopecia areata may be associated with autoimmune diseases such as vitiligo, pernicious anemia, collagen disease, and endocrinopathies. The characteristic histologic changes suggest an autoimmune etiology, but immunofluorescence studies have not revealed any evidence of bound antibody and no circulating antibodies to hair follicles have been demonstrated.
Traumatic alopecia is induced by physical trauma, of which the two most important groups, from the therapeutic standpoint are trichotillomania and alopecia resulting from cosmetic procedures or improper hair care. Trichotillomania is a compulsive habit in which the individual repeatedly pulls or breaks off his or her own hair in a partially conscious state similar to thumb sucking or nail biting. Clinically, this form of alopecia is characterized by an ill-defined patch on which the hairs are twisted and broken at various distances from the scalp surface. The scalp and hairs look otherwise normal. Other hairy areas of the body like the eyebrows and pubic region can be targets for this type of manipulation.
Traumatic alopecia from cosmetic procedures is done consciously in ill-advised individuals and is almost exclusively seen among females. The clinical pattern in these cases will be dictated by the different types of manipulation performed and it requires the suspicion of the observer. For example, traction alopecia from hair strengtheners and from brushes with synthetic fibers may produce alopecia in the temporofrontal regions, while traction alopecia from combs and rollers could affect the vertex and parietal regions. Sometimes this type of alopecia is associated with folliculitis induced by the occlusive effect of the oily cosmetics used in the procedure.
Anagen effluvium is a temporary alopecia caused by the inhibition of mitosis in the hair papilla by certain cytotoxic drugs, leading to constriction of the hair shaft or to complete failure of hair formation. The narrow hair shaft breaks easily and produces a characteristic pattern of tapered hairs that uniformly fracture at the same distance from the skin surface. Typically this effect will be evident from 10 days to 6 weeks after the administration of the cytotoxic agent and will resolve gradually upon discontinuation of the medication. Treatment is not necessary, but the patient should be apprised of the problem.
Alopecia may also result from nutritional deficiencies and metabolic defects. Caloric deprivation must be very severe to produce hair loss. Increased shedding sometimes occurs after marked weight loss for obesity. Anemia, diabetes, hyper- and hypovitaminosis, and zinc deficiency may also lead to alopecia.
Unfortunately, treatment for androgenetic alopecia has been ineffective in inducing regrowth. The use of cyclic estrogen therapy in females with an estrogen-dominant contraceptive or topical estrogen has been advocated to reduce the rate of hair loss, but results are not impressive. The claim that topical testosterone induces the growth of terminal hairs in bald scalp of males has not been confirmed.
In Europe, cyproterone acetate, an antiandrogen chemical that blocks the binding of testosterone by target-cell receptors, has been used combined with ethinylestradiol in females with androgenetic alopecia and found to reduce the rate of telogen shedding and stimulate more regrowth of terminal hairs. It seems that until the effectiveness of this treatment is finally assessed, the side effects and risks (dysmenorrhea, breast tenderness, headache, decreased libido, hepatitis, thrombophlebitis) outweigh its therapeutic effects.
Hair transplants have been used for several years as a corrective procedure for balding men based on the principle that the hair follicles on the occipital region are not under the same influence of androgens as the follicles in the balding area and once transplated will retain the capability of growth. It is a tedious and expensive procedure that requires the expertise of a skilled physician and the motivation and tolerance of the patient. This treatment is usually not indicated for females with androgenetic alopecia, since the loss of hair is too diffuse.
There have been some indications that minoxidil (Rogaine.RTM., Upjohn), a potent vasodilator, has been effective in causing scalp hair regrowth in patients with androgenetic alopecia, but the results have been mixed.
This invention relates to a composition of matter, and a method for applying same, useful as a hair grooming aid and as an effective method in the treatment of androgenetic alopecia.